If you think it can’t be done, think again. While you can still think.

Since the start of the COVID-19 outbreak that has now killed 214,000 Americans and 1-million people worldwide, doctors and clinicians gravitated to a unique artifact in the virus’s physiological onslaught in the body, namely in the pathogen’s deadly ability to affect vasopressor responses in the alveoli of the lungs, the tiny air sacs where site specific blood pressure levels are regulated to allow efficient oxygen-carbon dioxide exchange to facilitate the breath-by-breath oxygen-to-hemoglobin transport that keeps cells alive.

In those with acute respiratory symptoms, COVID-19 causes elevated blood pressure at the alveoli interfering directly with the critical gas exchange process at the cellular level, keeping oxygen from being adequately absorbed in the spongey tissues that make breathing possible.

Long story short, vasopressin is a necessary neurotransmitter for the maintenance of polite human society.

In laymen’s terms, if this crucial vasopressin-AVPR1A conjunction is disrupted by even minute variations in chemical coding, human beings become less able to regulate their emotions, including anger, frustration and irritation. This leads to activation of a specific structure in the brain involved in our rage and “fight or flight” response. The amygdala.

This makes vasopressin a virtual skeleton key in the turning off of key social responses that form the defining lines between love and hate and even a desire to either perpetuate or terminate the human species on the whole. In ways that are still not fully understood, vasopressin inflects our ability to value one another as human beings, to recognize that value on an individual and societal level and to make behavioral regulatory decisions on the basis of mutually perceived value and worth of human existence.

Other biochemical research studies have focused on the vasopressin-AVPR1A role in both male and female predilections for monogamy and infidelity, promiscuity and celibacy, with documented identifiable genetic markers in mating behaviors capable of predicting suitability for long term romantic couplings.

In simplest terms, vasopressin makes it possible for us to care about each other. Any interference with normative vasopressin response is a very bad thing, conceivably producing humans that are less empathetic and less instinctually committed to their own survival and to the preservation of the species.

In vasopressin-AVPR1A deficiencies already classified on the autistic spectrum, patients are less capable of receiving and expressing affection, less needful of human connection and less able to keep even low level frustrations from tipping over into episodic rage or panicked expressions of extreme fear and anxiety, with consequences that range from challenging to entirely unmanageable for families and communities.

There have been no scientific descriptions thus far on the specific interactions of COVID-19 on overall human vasopressin response and long term impacts on behavioral regulation in the human brain.

But even cursory analysis would suggest that a virus capable of rendering human beings more anxious, more fearful, more angry and less relatable to those around them and less defensive to species extinction would be a profoundly impactful piece of social engineering, in a virus already identified as a manmade chimera pathogen that evidence suggests was released intentionally by an enemy nation.

RNA-viral potentials as an undetectable packet delivery system for bioengineering of the human species are virtually unlimited in scale. And that knowledge base will only expand those horizons.

Could what initially appeared a killer pneumonia actually be a hyper-contagious carrier for a neurological “rage virus” or “empathy eraser” attacking a critical chemical in the regulation of fragile human society?

I’ll let you think about it. While you still can.